ArticleEMBO molecular medicine2015
Alzheimer-associated Aβ oligomers impact the central nervous system to induce peripheral metabolic deregulation.
Article in EMBO molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed, 216 citations in OpenAlex.
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- Visceral adipose tissue differentially affects tau and Aβ pathology in 3xTg-AD mice.Cell communication and signaling : CCS · 2026Article
- Inflammatory Signatures and Biomarkers: The Renal-Vesical Axis in Alzheimer Progression.International neurourology journal · 2026Article
- PTP1B inhibition promotes microglial phagocytosis in Alzheimer's disease models by enhancing SYK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Soluble and plaque amyloid associations with peripheral glucose dysregulation modulated by tau pathology in Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2026Observational
- Exploring the Impact of 3-Pharmaceuticals (Basel, Switzerland) · 2025Article
- Central Zika virus infection causes hypothalamic inflammation and persistent insulin resistance in adult mice.Cell death & disease · 2025Article
- Experimental menopause in 3xTg-AD mice exacerbates metabolic, inflammatory, and osteologic phenotypes aligned with Alzheimer's disease pathology.Research square · 2025Article
- Neural Metabolic Networks: Key Elements of Healthy Brain Function.Journal of neurochemistry · 2025Review
- Targeting CD38 immunometabolic checkpoint improves metabolic fitness and cognition in a mouse model of Alzheimer's disease.Nature communications · 2025Article
- Can infliximab serve as a new therapy for neuropsychiatric symptoms?Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- BACE1 at the crossroads of a vicious circle between Alzheimer's disease and diabetes mellitus.Frontiers in dementia · 2025Review
- Review
- Physiopathological Roles of White Adiposity and Gut Functions in Neuroinflammation.International journal of molecular sciences · 2024Review
- Peripheral inflammation is associated with brain atrophy and cognitive decline linked to mild cognitive impairment and Alzheimer's disease.Scientific reports · 2024Article
- The role of AMPKα subunit in Alzheimer's disease: In-depth analysis and future prospects.Heliyon · 2024Review
- Liver-specific adiponectin gene therapy suppresses microglial NLRP3-inflammasome activation for treating Alzheimer's disease.Journal of neuroinflammation · 2024Article
- Tauroursodeoxycholic acid: a bile acid that may be used for the prevention and treatment of Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Patient-derived tau and amyloid-β facilitate long-term depressionBrain communications · 2024Article
- Exercise Intervention for Alzheimer's Disease: Unraveling Neurobiological Mechanisms and Assessing Effects.Life (Basel, Switzerland) · 2023Review
50 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is associated with peripheral metabolic disorders. Clinical/epidemiological data indicate increased risk of diabetes in AD patients. Here, we show that intracerebroventricular infusion of AD-associated Aβ oligomers (AβOs) in mice triggered peripheral glucose intolerance, a phenomenon further verified in two transgenic mouse models of AD. Systemically injected AβOs failed to induce glucose intolerance, suggesting AβOs target brain regions involved in peripheral metabolic control. Accordingly, we show that AβOs affected hypothalamic neurons in culture, inducing eukaryotic translation initiation factor 2α phosphorylation (eIF2α-P). AβOs further induced eIF2α-P and activated pro-inflammatory IKKβ/NF-κB signaling in the hypothalamus of mice and macaques. AβOs failed to trigger peripheral glucose intolerance in tumor necrosis factor-α (TNF-α) receptor 1 knockout mice. Pharmacological inhibition of brain inflammation and endoplasmic reticulum stress prevented glucose intolerance in mice, indicating that AβOs act via a central route to affect peripheral glucose homeostasis. While the hypothalamus has been largely ignored in the AD field, our findings indicate that AβOs affect this brain region and reveal novel shared molecular mechanisms between hypothalamic dysfunction in metabolic disorders and AD.
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